Objective To investigate the relationship between obstructive sleep apneahypopnea syndrome (OSAHS) and carotid stenosis in patients with ischemic cerebrovascular disease (ICVD) and to provide reference for developing the intervention strategy of carotid stenosis. Methods Eighty-seven patients with ICVD were screened from Nanjing Stroke Registry Program. The patients were divided into without (n=21), mild(n=24), moderate (n=27) and severe (n = 11) OSAHS groups according to the apnea-hypopnea index (AHI); in addition, the patients were divided into with (n =34) and without carotid stenosis (n=49) groups according to the results of digital subtraction angiography (DSA). The effects of the risk factors for cerebrovascular diseases and OSAHS on carotid stenosis in patients with ICDV were analyzed.Results There were significant differences in the proportions of alcohol consumption (χ2=8.56, P =0. 036), hypertension (χ2 = 13.20, P =0. 004) and carotid stenosis (χ2 =22.97, P =0. 006) between the no OSAHS and the mild, moderate and severe OSAHS groups. The univariate analysis showed that age (OR = 1. 066, 95% CI 1. 023- 1.112; P = 0. 003),hypertension (OR =3.587, 95% CI 1. 294- 9. 949; P =0. 014), alcohol consumption (OR =5.275,95% CI 1.855-15.001; P= 0.002) and OSAHS (OR= 1.073, 95% CI 1.033-1.115; P = 0. 000) were the risk factors for carotid stenosis. The multivariate logistic regression analysis showed that age (OR = 1. 113, 95% CI 1. 047-1. 182; P =0. 001), OSAHS (OR = 1. 096, 95% CI 1. 034-1. 160; P = 0. 000), and alcohol consumption (OR = 4. 292,95% CI 1. 217-15. 139; P = 0. 024) were the independent risk factors for carotid stenosis.Spearman rank correlation analysis suggested that the AHI levels were positively correlated with the degree of carotid stenosis (r = 0. 435, P = 0. 000). There were significant differences among the without stenosis (n =34), unilateral stenosis (n =22), and bilateral stenosis (n=27)groups (12.97 ± 10.04 vs. 21.40 ± 16.38 vs. 29.33 ± 13.81, F= 11.64, P<0.01).Conclusions OSAHS is an independent risk factor for carotid stenosis and it was positively correlated with the severity of carotid stenosis. AHI may reflect the degree of carotid stenosis and the range of neck vascular involvement to some extent.

Objective To study the expression of lipoic acid synthase(LIAS)in the liver and kidney of Leprdb/db mice with deficient leptin receptor. Methods Eight 10-week old male Leprdb/ +mice and Leprdb/dbmice were included in this study. The body weight of rats in the two groups was measured. Fasting blood glucose(FPG)was measured with blood glucose test strips for all mice after fasting for 8 hours. Blood samples were obtained from the abdominal aorta and the animals were sacrificed. The liver and kidney were weighed. The right lobe of liver and the left kidney samples were fixed in 4% paraformaldehyde for pathological examination. Serum samples were separated and the sereum contents of CHO, TG,HDL and LDL were detected. The mitochondria of liver and kidney tissues were extracted with a mitochondrial isolation kit, and the protein was extracted. The expression of LIAS protein was detected by western blot. Results Histopathological observation showed that the liver and kidney tissues of Leprdb/ +mice have intact and clear structure. But the liver tissue of Leprdb/dbmice showed fatty degeneration, the kidney tissue showed glomerular hypertrophy, basement membrane thickening, mesangial area widened, including mesangial cells and mesangial matrix increased. The GLU,CHO,TG,LDL and AST of Leprdb/dbmice were significantly increased compared with those of Leprdb/ +mice(P<0.05). Compared with Leprdb/ +mice,the LIAS protein expression was significantly increased in the liver and kidney mitochondria of Leprdb/dbmice(P<0.05). Conclusions There is impaired glucose and lipid metabolism in the Leprdb/dbmice which has defect leptin receptor,and the expression of LIAS protein in liver and kidney of the Leprdb/dbmice is higher than that of Leprdb/ +mice.

Objective To establish an efficient method of genotyping for Leprdb/ +mouse offsprings by TaqMan probe quantitative fluorescence PCR. Methods Genome DNA was extracted from tails of 228 Leprdb/ +mouse offsprings. PCR primers and TaqMan probes were designed according to the mutation sites of Lepr gene(rs1801133). Real time PCR assay was applied and SNP loci were typed with SDS software. The genotyping of 2-month old Leprdb/dbmice was validated by the phenotype and Hardy-Weinberg equilibrium test was performed. Results 228 samples were detected by the established TaqMan fluorescence quantitative PCR assay. 64 mice were of GG genotype, with a genotype frequency of 0.1929. 123 mice were of GT genotype, with a genotype frequency of 0.5395. 41 mice were of TT genotype, with a genotype frequency of 0.2807. Compared with the phenotype typing,the sensitivity of the TaqMan fluorescence quantitative PCR was 97.56% and the specificity was 99.47%. Conclusions TaqMan probe quantitative fluorescence PCR assay is a simple and efficient method,and can be used to detect the genotype of Leprdb/ +mouse offsprings.

Objective: To analyze the normal value of the iodine content in the left ventricular myocardium of healthy subjects and to observe if there is a segmental differences on iodine distribution by using the second generation dual-source dual-energy computed tomography myocardial first perfusion imaging. Methods: In this retrospective study, 42 healthy subjects, who admitted to our department between January to June 2016, with normal second generation dual-source dual-energy computed tomography and coronary CT angioghphy (CTA), electrocardiogram (ECG) results, normal cardiac, hepatic, renal function, normal myocardial enzymes results were enrolled, data from 38 out of 42 subjects with satisfactory image quality were analyzed using Siemens Dual Energy-Heart PBV image processing software.In accordance with the standards of the American Heart Association myocardial 17 fractionation method, content of iodine was measured at different segmental left ventricular myocardium and aorta (left coronary artery from the opening level). The standardized containing iodine value (nIC) was calculated. Results: The iodine content of left ventricular myocardium in normal subjects was 3.1-7.8 mg/ml.The nIC of myocardium from 1st to 17th segments was 0.28±0.06, 0.31±0.07, 0.30±0.07, 0.30±0.04, 0.28±0.04, 0.29±0.05, 0.29±0.01, 0.30±0.07, 0.31±0.07, 0.27±0.06, 0.28±0.08, 0.28±0.07, 0.29±0.08, 0.31±0.07, 0.27±0.06, 0.29±0.06 and 0.21±0.07, respectively.The nIC of the 17th segment was the lowest and was significantly lower than in other segments (all P<0.05), the nIC was similar among the rest 16 segments (all P>0.05). Conclusion The normal iodine content range in left ventricle myocardium is 3.1-7.8 mg/ml, and the lowest iodine content is detected in the apex and which is significantly lower than the other left ventricular segments.

Platelet-rich fibrin(PRF) was first reported in 2001 by Choukroun. PRF is rich in growth factors, which can promote collagen deposition, angiogenesis, and reduce the incidence of postoperative pain, inflammatory reaction and infection. It is often used in stomatology and other wound repair. Recently, some researchers try to use PRF in fat grafting. The aim of this review is to summarize PRF and its application in fat grafting.

Objective To explore the effects of ADAR1 inducer and inhibitor on cognition and ADAR1 expression of isolated BALB/c mice.Methods Sixty healthy BALB/c mice were divided into 6 groups according to randomized design with 10 animals each group,the gregarious control group (GH),social isolation model group (SI),ADAR1 inducer treated gregarious group (GH+IFN-γ),ADAR1 inhibitor treated gregarious group (GH+EHNA),ADAR1 inducer treated isolation group (SI+IFN-γ) and ADAR1 inhibitor treated isolation group (SI+EHNA).Mice in drug treatment groups were treated with ADAR1 inducer (5.0? 104 U/kg,20 ml/kg,ip) and inhibitor (10 mg/kg,20 ml/kg,ip).Objection recognition test was used to measure cognition.Immunohistochenmistry was used to measure ADARI immunoreactivity and Western blotwas used to measure ADAR1 protein expression.Results In the objection recognition test,the non-spatial discrimination index of mice in SI group (-0.16±0.09) was significantly lower than that of GH group (0.41 ±0.17,P＜0.01),the non-spatial discrimination index of mice in SI+IFN-γ group (0.20±0.09) and in SI+ EHNA group (-0.29±0.12) was higher (P＜0.01) and lower (P＜0.05) than that of the SI group respectively.The immunohistochemistry results showed that the ADAR1 immunoreactivity in hippocampus of mice in SI group (Hilus:(0.013±0.003),CAI:(0.021±0.005)) decreased significantly compared to those of GH group(Hilus:(0.021 ±0.002),(0.047±0.004);both P＜0.05).And GH+IFN-γgroup mice showed increased ADAR1 immunoreactivity obviously in Hilus ((0.013±0.003) vs (0.023±0.004),P＜0.01) and in CA1 ((0.021±0.005) vs (0.040±0.005),P＜0.01) compared with that of SI group,ADAR1 inducer recovered the above abnornal ADAR1 immunoreactivity.Western blot results showed that the ADAR1 protein expression of mice in SI group (0.48 ±0.07) in hippocampus was significantly decreased (P＜0.01) compared to that of GH group (1.00 ±0.00).The level of ADAR1 protein in SI+IFN-γgroup(0.82 ±0.04) increased compared with that of SI group.Conclusions Four weeks of social isolation can reduce the non-spatial cognitive ability of BALB/c mice and decrease the expression of ADAR1 in the hippocampus.The ADAR1 inducers and inhibitors can reverse and aggravate the cognitive impairment caused by social isolation respectively.The related mechanisms may be related to the expression of ADAR1.

Objective: To explore the application of the 3D precise digital technology in restoring structural defects of the orbital region. Methods: Structural defects of the orbital region concerning on osseous structure and soft tissue were restored in one stage or stages using EH composite artificial bone prosthesis with complex three-dimensional structure. The fabrication of EH composite artificial bone prosthesis was based on CT scanning and 3D reconstruction of the skull with computer aided data analysis and design. The appearance, degree of satisfaction and the complications were evaluated in postoperative regular follow-up. Results: Five cases of structural defects in the orbital regions presenting bone defect and soft tissue abnormality, received treatments in the department from January 2016 to September 2017. The cases consist of one patient with dysplasia following surgical treatment, three with post-traumatic and one with Treacher-Collins syndrome. With the application of individualized EH composite artificial bone fabricated by aforementioned method, all the repair materials presented the ideal three-dimensional structure and coincided well with the defects, and soft tissue restoration of 2 cases was performed in one stage or by stages. Appearance and symmetry of the 5 cases was significantly improved, without complications of infection, rejection, exposure or graft tissue necrosis. All the patients were satisfied with the results. Conclusions In consideration of the capacity to fabricate accurate individualized repair materials, the three-dimensional digital technology plays an important role in the treatment of structural defects in the orbital region, especially the reconstruction of the bony contour. The simple orbital deformities can be treated with the repair materials and correction of soft tissue. For special orbital deformities, attention should be paid to bone structure repair, eye socket reconstruction and filling of orbital contents sequentially.

Objective:To investigate the effect of adenosine deaminase acting on RNA 1 (ADAR1) on 5-serotonin-2c receptor in alleviating aggression in socially isolated mice.Methods:Sixty healthy male BALB / c mice aged 21 days were randomly divided into six groups: social isolation group, social control group, ADAR1 inducer social isolation group, ADAR1 inhibitor social isolation group, ADAR1 inducer social control group and ADAR1 inhibitor control group.The mice fed in single cage for 4 weeks were used as social isolation model while the mice fed in group were used as control group.ADAR1 inducer (5.0×10 4 U/kg) and inhibitor (10 mg/kg) were given intraperitoneally to mice in the ADAR1 inducer social isolation group and the ADAR1 inhibitor social isolation group respectively.The aggressive behavior of mice was evaluated by resident-intruder test.The expression of ADAR1 and 5-serotonin-2c receptors in the brain of mice was detected by immunohistochemistry and Western blot. Results:The attack latency of social isolation group was significantly lower than that of social control group ((43.15±6.99) s, (542.40±30.50) s; t=15.906, P<0.01), and the latency of attack ((256.70±29.49) s) in the ADAR1 inducer social isolation group was significantly higher than that in the social isolation group ( t=7.046, P<0.01). The latency of attack ((15.25±2.18)s) in the ADAR1 inhibitor social isolation group was significantly lower than that in the social isolation group ( t=3.809, P<0.01). The optical density of ADAR1 immunoreactive cells in the amygdala of the social isolation group mice was significantly lower than that in the corresponding brain area of the social control group (BLA: (0.038±0.002), (0.074±0.004); LaDL: (0.033±0.002), (0.060±0.002); LaVM: (0.045±0.003), (0.073±0.004); Lavl area: (0.044±0.003), (0.070±0.003); t=8.428, 9.037, 6.462, 5.698, all P<0.01). The optical density of ADAR1 immunoreactive positive cells in the amygdala (BLA: (0.060±0.003), LaDL: (0.042±0.002), LaVM: (0.056±0.004), Lavl: (0.054±0.003) in the ADAR1 inducer social isolation group was significantly higher than those in the corresponding brain area of the social isolation group mice ( t=6.055, 2.876, 2.312, 2.492; all P<0.05). The expression of ADAR1 protein and 5-serotonin-2c receptor protein in amygdala of social isolation group were significantly lower than those of social isolation group ( t=11.37, 12.65; P<0.01). The expression of ADAR1 protein and 5-serotonin-2c receptor protein in the amygdala of the ADAR1 inducer social isolation group were significantly higher than those of the social isolation group ( t=3.02, 4.401; P<0.05). Conclusion:ADAR1 inducer alleviates the aggressive behavior of social isolated BALB / c mice by enhancing the protein expression of 5-serotonin-2c receptor in the amygdala of social isolated BALB/c mice.